Glaucoma is an optic neuropathy characterized by acquired atrophy of the optic nerve and loss of retinal ganglion cells and their axons. Among other factors, elevated intraocular pressure contributes to progressive irreversible optic nerve damage and visual field loss, which may lead to complete blindness.
Worldwide, glaucoma is the second leading cause of blindness. Glaucoma affects 1 in 200 people aged fifty and younger, and 1 in 10 over the age of eighty. If the condition is detected early enough it is possible to stop the development or at least slow the progression of glaucoma with medical and surgical means.
Glaucoma is associated with increased pressure (intraocular pressure) of the liquid (aqueous humor) in the anterior chamber of the eye. There are many different sub-types of glaucoma but they can all be considered a type of optic neuropathy. Raised intraocular pressure is a significant risk factor for developing glaucoma (above 21 mmHg or 2.8 kPa). It is noted that nerve damage may develop due to increase in the intraocular pressure, however the magnitude of increased pressure that may cause nerve damage is individual, i.e. for certain people a relatively small increase in the intraocular pressure may result in irreversible nerve damage, while other people may have high eye pressure for long periods of time (i.e. months or years) before developing nerve damage. Untreated glaucoma leads to permanent damage of the optic nerve fibers and progressive visual field loss, which can lead to complete blindness.
Glaucoma can be divided roughly into two main categories, “open angle” glaucoma (OAG) and “closed angle” glaucoma (CAG). CAG can appear suddenly, leading to excruciating pain, or insidiously with minimal discomfort. In the acute form visual loss can progress quickly but the discomfort often leads patients to seek medical attention before permanent damage occurs. OAG and chronic angle closure glaucoma tends to progress at a slower rate and the patient may not notice that they have lost vision until the disease has progressed significantly.
The intraocular pressure is maintained by the dynamic equilibrium of aqueous production and outflow. The iris divides the anterior portion of the eye into anterior and posterior chambers, which communicate through the pupil. Aqueous humor, produced by the ciliary body, fills the posterior chamber, flows through the pupil into the anterior chamber, and leaves the eye through the trabecular meshwork, a connective tissue filter at the angle between the iris and the cornea. The aqueous humour passes through the trabecular meshwork into Schlemm's canal and into the episcleral venous system. Increased intraocular pressure is caused by obstruction to outflow. In OAG conditions, obstruction exists at a microscopic level in the trabecular meshwork. In CAG the iris obstructs the trabecular meshwork physically either because of anatomic variation leadingto pupillary block and obstruction of aqueous humor flow into the anterior chamber, or by formation of adhesions between the iris and trabeculum.
There are a number of known devices intended to control the intraocular pressure in glaucomatotic eyes:
U.S. Pat. No. 5,300,020 discloses a surgically implantable device for controlled drainage flow of aqueous fluid from the anterior chamber of the eye into nearby sub-conjunctival space, for the relief of a glaucomatous condition of excessive pressure within the eye. The porous material in the device of U.S. Pat. No. 5,300,020 is indicated to be biodegradable, thus within a matter of time this material is decomposed, leaving a hollow tube connecting the anterior chamber with the near sub-conjunctival space. The purpose and effect of the biodegradability of the porous material inside the device is to avoid early hypotony. However, this device will not be able to improve surgical outcome since draining fluid to the near subconjuctival space will be able to relieve intraocular pressure for a short period of time. With time scar tissue will develop in a percentage of patients thus clogging the device and conjunctival bleb.
U.S. Pat. No. 5,743,868 discloses a unitary, pressure-regulating corneal implant device for use in controlling intraocular pressure. This implant, having a conduit with a bore and a porous core material disposed in the bore, allows egress of aqueous humor from the anterior chamber of the eye. The conduit is elongated for extending from the ocular surface of the eye substantially flush therewith through the corneal stroma, and into the anterior chamber. This is an open system device, thus allowing egress of fluid into the eye possibly containing infections agents. Cornea will most probably reject the device as a foreign body (usually the case when implanting a body into the cornea) and also distorts the optical surface of the cornea thereby giving rise to optical aberations to patients treated with this device.
U.S. Pat. No. 4,946,436 relates to a porous device for implantation in the scleral tissue of the eye to relieve the intraocular pressure of glaucoma and a method for surgically implanting the device. It is noted that such devices are intended for being implanted intrasclerally and thus will be able to remove the fluid only to the subsidiary space. Devices described in U.S. Pat. No. 4,946,436 were not found to improve surgical results when compared with trabeculectomy, where treating glaucoma.